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Aberrant T-cell phenotypes in a cohort of patients with post-treatment Lyme disease Alexander A. Girgis, Raffaello Cimbro, Ting Yang, Alison W. Rebman, Thelio Sewell, Daniela Villegas de Flores, Aarti Vadalia, William H. Robinson,, Andrea L. Cox, Erika Darrah, Mark J. Soloski, John Aucott...

SARS-CoV-2 Semi-Quantitative Total Antibody Correlates with Symptoms of Long COVID in Both Vaccinated and Unvaccinated Subjects James R White, Ralph L Abraham, Wyche Coleman,Eddie Pitre, Megan M Stevenson, Hannah L Kaplan, Alexander G Goldberg, Molly A. Allen, Cecilia A. Castro, Abby A. Haddox...

Similar authors and scope to this other recent paper: Cost effectiveness of non-pharmacological interventions for fatigue in patients with long-term conditions: a systematic literature review, 2025 Davis+

Effectiveness of non-pharmacological Interventions For Fatigue in Long term conditions (EIFFEL) - systematic review and network meta-analysis Joanna Leaviss, Christopher Burton, EIFFEL study group, University of Sheffield [Line breaks added] Objective To assess the clinical effectiveness of...

Yes, my main fear that prompted the post was the ambiguity of, for example, an HLA allele finding. It might just cause people to get sick more severely and more often, which doesn't really seem that interesting in terms of how to treat ME/CFS if the subsequent disease process has nothing to do...

Very good points. It might be more trouble than it's worth if it only controls for a tiny portion of the phenomenon.

Good question, I'm not sure how correction would work in that case.

Yeah, there are various questions, and why the best approach would just be to record that data on severity, but not perfectly match groups. You can do an uncontrolled analysis, but also do an analysis with severity as a covariate.

Practically, if you're just using any and all ME/CFS cases, there's not really any way to control for severity since everyone has had lots of different infections. So this doesn't really apply, and maybe it would still just be better to use the heterogenous cohort to not get microbe-specific...

I think you're reading it backwards. The most recent dates are on the left.

Rate of 4.5% Post-COVID ME/CFS Onset Cited in Recent RECOVER Study is Based on Biased Cohort Arther A. Mirin [Letter to the editor. This is the whole letter.] The recent paper by Vernon, et al.1 predicts that 4.5% of adult COVID sufferers in the United States experience subsequent onset of...

Yes, the processes of the acute illness are important. I think what I'm mainly suggesting is, if you are able to study them separately in order to make it easier to match gene to specific process, why not do that? Why not have one cohort that outwardly had identical infections, then a week...

Actually, maybe the heterogeneity of different infections preceding ME/CFS achieves a similar goal. If you only look at post-COVID ME/CFS, then, even if matching for severity, there might be a lot of COVID specific genes that have nothing to do with the common processes underlying ME/CFS after...

I'm having a hard time following. If you don't want to deliberately pick cases and controls with different severities, then clearly it's a confounder so why not match severity as closely as possible. But neither of these sounds like it gets the heart of ME/CFS. It might provide some interesting...

Yes, that's mainly what I'm arguing for, and something that's not possible if you are using ME/CFS cases that followed a hodge podge of other infections. Sure, that may be unavoidable, and may be interesting anyway.

Yes, mostly I was thinking about avoiding having controls who have never had an infection at all. So maybe not a big concern. It slipped my mind that 90% of people have EBV in their system. Still, while the science might not be settled, a lot of studies are finding that initial COVID severity...

RECOVER is doing genetic testing on a lot of people with long COVID (~14k), so maybe they will do some ME/CFS-specific analysis versus recovered controls.